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作 者:Nan Yin Dan Zhang Jiqiu Wang
机构地区:[1]Department of Endocrine and Metabolic Diseases,Shanghai Institute of Endocrine and Metabolic Diseases,Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 200025,China [2]Shanghai National Clinical Research Center for Metabolic Diseases,Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the People’s Republic of China,Shanghai National Center for Translational Medicine,Shanghai 200025,China [3]Department of Pediatric Endocrine and Metabolic Diseases,Shengjing Hospital of China Medical University,Shenyang,Liaoning 110801,China
出 处:《Life Metabolism》2024年第6期50-53,共4页生命代谢(英文)
基 金:supported by grants from the National Natural Science Foundation of China(91957124 to J.W.);the National Key Research and Development Program of China(2022YFC2505201 to J.W.).
摘 要:Dear Editor,Genome-wide association studies(GWAS)revealed a large number of common variants in the human genome associated with an increased risk of diseases.The lead signals of common obesity-associated variants are located within the first intron of the FTO(fat mass and obesity-associated)gene,being the most significant and impactive single-nucleotide polymorphism(SNP)clusters in obesity inheritance[1].Although a strong positive association between these FTO“risk SNPs”(including rs1421085 T>C)and obesity is reported across human populations of diverse ancestry,relatively weak(even none)significant associations have been observed in African populations[2].As known,the frequency of the FTO SNPs varies among different ancestral groups,with the“risk allele”being prevalent in individuals of European ancestry and less common in Asian and African populations.Notably,the linkage disequilibrium(LD)of the“risk SNPs”in African populations was much lower than in non-African populations[3].The reason for the discrepancy remains elusive thus far;however,it could be redefined in the context of the unexpected biological function of the FTO SNPs in vivo[4].
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